Background

Recent analysis has demonstrated a remarkably consistent, nonlinear relationship between estimated inhaled dose of combustion particles measured as PM(2.5) (particulate matter with aerodynamic diameter ≤ 2.5 µm) and cardiovascular disease mortality over several orders of magnitude of dose--from cigarette smoking, environmental tobacco smoke (ETS) exposure, and ambient air pollution exposure.

Objectives

Here we discuss the implications of this relationship and point out the gaps in our knowledge that it reveals.

Discussion

The nonlinear exposure-response relationship that is revealed-much steeper at lower than at higher doses-explains the seemingly inconsistent risks observed from ambient air pollution and cigarette smoking but also raises important questions about the relative benefits of control at different points along the curve. This analysis also reveals a gap in the evidence base along the dose-response curve between ETS and active smoking, which is the dose range experienced by half the world's population from indoor biomass and coal burning for cooking and heating.

Conclusions

The shape of the exposure-response relationship implies much larger public health benefits of reductions at the lower end of the dose spectrum (e.g., from reductions in outdoor air pollution) than from reducing the rate of active smoking, which seems counterintuitive and deserving of further study because of its importance for control policies. In addition, given the potential risks and consequent global disease burden, epidemiologic studies are urgently needed to quantify the cardiovascular risks of particulate matter exposures from indoor biomass burning in developing countries, which lie in the dose gap of current evidence.

Background: Exposure to household air pollution generated as a result of cooking and heating is a leading contributor to global disease. The effects of cookstove-generated air pollution on adult lung function, however, remain uncertain.Objectives: We investigated acute responses in lung function following controlled exposures to cookstove-generated air pollution.Methods: We recruited 48 healthy adult volunteers to undergo six two-hour treatments: a filtered-air control and emissions from five different stoves with fine particulate matter (PM_2.5) targets from 10 to 500 µg/m³. Spirometry was conducted prior to exposure and immediately, and three and 24 h post-exposure. Mixed-effect models were used to estimate differences in post-exposure lung function for stove treatments versus control.Results: Immediately post-exposure, lung function was lower compared to the control for the three highest PM_2.5-level stoves. The largest differences were for the fan rocket stove (target 250 µg/m³; forced vital capacity (FVC): -60 mL, 95% confidence interval (95% CI) -135, 15; forced expiratory volume (FEV₁): -51 mL, 95% CI -117, 16; mid-expiratory flow (FEF_25-75): -116 mL/s, 95% CI -239, 8). At 3 h post-exposure, lung function was lower compared to the control for all stove treatments; effects were of similar magnitude for all stoves. At 24 h post-exposure, results were consistent with a null association for FVC and FEV₁; FEF_25-75 was lower relative to the control for the gasifier, fan rocket, and three stone fire.Conclusions: Patterns suggesting short-term decreases in lung function follow from exposure to cookstove air pollution even for stove exposures with low PM_2.5 levels.

Household air pollution is a leading risk factor for morbidity and premature mortality. Numerous cookstoves have been developed to reduce household air pollution, but it is unclear whether such cookstoves meaningfully improve health. In a controlled exposure study with a crossover design, we assessed the effect of pollution emitted from multiple cookstoves on acute differences in blood lipids and inflammatory biomarkers. Participants (n = 48) were assigned to treatment sequences of exposure to air pollution emitted from five cookstoves and a filtered-air control. Blood lipids and inflammatory biomarkers were measured before and 0, 3, and 24 hours after treatments. Many of the measured outcomes had inconsistent results. However, compared to control, intercellular adhesion molecule-1 was higher 3 hours after all treatments, and C-reactive protein and serum amyloid-A were higher 24 hours after the highest treatment. Our results suggest that short-term exposure to cookstove air pollution can increase inflammatory biomarkers within 24 hours.

Background Exposure to air pollution from solid fuel used in residential cookstoves is considered a leading environmental risk factor for disease globally, but evidence for this relationship is largely extrapolated from literature on smoking, secondhand smoke, and ambient fine particulate matter ( PM _2.5). Methods and Results We conducted a controlled human-exposure study (STOVES [the Subclinical Tests on Volunteers Exposed to Smoke] Study) to investigate acute responses in blood pressure following exposure to air pollution emissions from cookstove technologies. Forty-eight healthy adults received 2-hour exposures to 5 cookstove treatments (three stone fire, rocket elbow, fan rocket elbow, gasifier, and liquefied petroleum gas), spanning PM _2.5 concentrations from 10 to 500 μg/m³, and a filtered air control (0 μg/m³). Thirty minutes after exposure, systolic pressure was lower for the three stone fire treatment (500 μg/m³ PM _2.5) compared with the control (-2.3 mm Hg; 95% CI, -4.5 to -0.1) and suggestively lower for the gasifier (35 μg/m³ PM _2.5; -1.8 mm Hg; 95% CI , -4.0 to 0.4). No differences were observed at 3 hours after exposure; however, at 24 hours after exposure, mean systolic pressure was 2 to 3 mm Hg higher for all treatments compared with control except for the rocket elbow stove. No differences were observed in diastolic pressure for any time point or treatment. Conclusions Short-term exposure to air pollution from cookstoves can elicit an increase in systolic pressure within 24 hours. This response occurred across a range of stove types and PM _2.5 concentrations, raising concern that even low-level exposures to cookstove air pollution may pose adverse cardiovascular effects.

Background

Exposure to household air pollution from solid fuel combustion for cooking and heating is an important risk factor for premature death and disability worldwide. Current evidence supports an association of ambient air pollution with cardiovascular disease but is limited for household air pollution and for cardiac function. Controlled exposure studies can complement evidence provided by field studies.

Objectives

To investigate effects of short-term, controlled exposures to emissions from five cookstoves on measures of cardiac function.

Methods

Forty-eight healthy adults (46% female; 20-36 years) participated in six, 2-h exposures ('treatments'), including emissions from five cookstoves and a filtered-air control. Target fine particulate matter (PM_2.5) exposure-concentrations per treatment were: control, 0 µg/m³; liquefied petroleum gas, 10 µg/m³; gasifier, 35 µg/m³; fan rocket, 100 µg/m³; rocket elbow, 250 µg/m³; and three stone fire, 500 µg/m³. Participants were treated in a set (pre-randomized) sequence as groups of 4 to minimize order bias and time-varying confounders. Heart rate variability (HRV) and cardiac repolarization metrics were calculated as 5-min means immediately and at 3 h following treatment, for analysis in linear mixed-effects models comparing cookstove to control.

Results

Short-term differences in SDNN (standard deviation of duration of all NN intervals) and VLF (very-low frequency power) existed for several cookstoves compared to control. While all cookstoves compared to control followed a similar trend for SDNN, the greatest effect was seen immediately following three stone fire (β = -0.13 ms {%}; 95% confidence interval = -0.22, -0.03%), which reversed in direction at 3 h (0.03%; -0.06, 0.13%). VLF results were similar in direction and timing to SDNN; however, other HRV or cardiac repolarization results were not similar to those for SDNN.

Discussion

We observed some evidence of short-term, effects on HRV immediately following cookstove treatments compared to control. Our results suggest that cookstoves with lower PM_2.5 emissions are potentially capable of affecting cardiac function, similar to stoves emitting higher PM_2.5 emissions.

Household air pollution emitted from solid-fuel cookstoves used for domestic cooking is a leading risk factor for morbidity and premature mortality globally. There have been attempts to design and distribute lower emission cookstoves, yet it is unclear if they meaningfully improve health. Using a crossover design, we assessed differences in central aortic hemodynamics and arterial stiffness following controlled exposures to air pollution emitted from five different cookstove technologies compared to a filtered air control. Forty-eight young, healthy participants were assigned to six 2-h controlled treatments of pollution from five different cookstoves and a filtered air control. Each treatment had a target concentration for fine particulate matter: filtered air control = 0 μg/m³, liquefied petroleum gas = 10 μg/m³, gasifier = 35 μg/m³, fan rocket = 100 μg/m³, rocket elbow = 250 μg/m³, three stone fire = 500 μg/m³. Pulse wave velocity (PWV), central augmentation index (AIx), and central pulse pressure (CPP) were measured before and at three time points after each treatment (0, 3, and 24 h). Linear mixed models were used to assess differences in the outcomes for each cookstove treatment compared to control. PWV and CPP were marginally higher 24 h after all cookstove treatments compared to control. For example, PWV was 0.15 m/s higher (95% confidence interval: -0.02, 0.31) and CPP was 0.6 mmHg higher (95% confidence interval: -0.8, 2.1) 24 h after the three stone fire treatment compared to control. The magnitude of the differences compared to control was similar across all cookstove treatments. PWV and CPP had no consistent trends at the other post-treatment time points (0 and 3 h). No consistent trends were observed for AIx at any post-treatment time point. Our findings suggest higher levels of PWV and CPP within 24 h after 2-h controlled treatments of pollution from five different cookstove technologies. The similar magnitude of the differences following each cookstove treatment compared to control may indicate that acute exposures from even the cleanest cookstove technologies can adversely impact these subclinical markers of cardiovascular health, although differences were small and may not be clinically meaningful.

Household air pollution is estimated to be responsible for nearly three million premature deaths annually. Measuring fractional exhaled nitric oxide (FeNO) may improve the limited understanding of the association of household air pollution and airway inflammation. We evaluated the cross-sectional association of FeNO with exposure to household air pollution (24-h average kitchen and personal fine particulate matter and black carbon; stove type) among 139 women in rural Honduras using traditional stoves or cleaner-burning Justa stoves. We additionally evaluated interaction by age. Results were generally consistent with a null association; we did not observe a consistent pattern for interaction by age. Evidence from ambient and household air pollution regarding FeNO is inconsistent, and may be attributable to differing study populations, exposures, and FeNO measurement procedures (e.g., the flow rate used to measure FeNO).

Household air pollution from solid cooking fuel use during gestation has been associated with adverse pregnancy and birth outcomes. The Household Air Pollution Intervention Network (HAPIN) trial was a randomized controlled trial of free liquefied petroleum gas (LPG) stoves and fuel in Guatemala, Peru, India, and Rwanda. A primary outcome of the main trial was to report the effects of the intervention on infant birth weight. Here we evaluate the effects of a LPG stove and fuel intervention during pregnancy on spontaneous abortion, postpartum hemorrhage, hypertensive disorders of pregnancy, and maternal mortality compared to women who continued to use solid cooking fuels. Pregnant women (18-34 years of age; gestation confirmed by ultrasound at 9-19 weeks) were randomly assigned to an intervention (n = 1593) or control (n = 1607) arm. Intention-to-treat analyses compared outcomes between the two arms using log-binomial models. Among the 3195 pregnant women in the study, there were 10 spontaneous abortions (7 intervention, 3 control), 93 hypertensive disorders of pregnancy (47 intervention, 46 control), 11 post postpartum hemorrhage (5 intervention, 6 control) and 4 maternal deaths (3 intervention, 1 control). Compared to the control arm, the relative risk of spontaneous abortion among women randomized to the intervention was 2.32 (95% confidence interval (CI): 0.60, 8.96), hypertensive disorders of pregnancy 1.02 (95% CI: 0.68, 1.52), postpartum hemorrhage 0.83 (95% CI: 0.25, 2.71) and 2.98 (95% CI: 0.31, 28.66) for maternal mortality. In this study, we found that adverse maternal outcomes did not differ based on randomized stove type across four country research sites.

Fine particulate air pollution <2.5 μm in diameter (PM_2.5) is a major environmental threat to global public health. Multiple national and international medical and governmental organizations have recognized PM_2.5 as a risk factor for cardiopulmonary diseases. A growing body of evidence indicates that several personal-level approaches that reduce exposures to PM_2.5 can lead to improvements in health endpoints. Novel and forward-thinking strategies including randomized clinical trials are important to validate key aspects (e.g., feasibility, efficacy, health benefits, risks, burden, costs) of the various protective interventions, in particular among real-world susceptible and vulnerable populations. This paper summarizes the discussions and conclusions from an expert workshop, Reducing the Cardiopulmonary Impact of Particulate Matter Air Pollution in High Risk Populations, held on May 29 to 30, 2019, and convened by the National Institutes of Health, the U.S. Environmental Protection Agency, and the U.S. Centers for Disease Control and Prevention.

Household air pollution (HAP) from cooking with solid fuels used during pregnancy has been associated with adverse pregnancy outcomes. The Household Air Pollution Intervention Network (HAPIN) trial was a randomized controlled trial that assessed the impact of a liquefied petroleum gas (LPG) stove and fuel intervention on health in Guatemala, India, Peru, and Rwanda. Here we investigated the effects of the LPG stove and fuel intervention on stillbirth, congenital anomalies and neonatal mortality and characterized exposure-response relationships between personal exposures to fine particulate matter (PM_2.5), black carbon (BC) and carbon monoxide (CO) and these outcomes. Pregnant women (18 to <35 years of age; gestation confirmed by ultrasound at 9 to <20 weeks) were randomly assigned to intervention or control arms. We monitored these fetal and neonatal outcomes and personal exposure to PM_2.5, BC and CO three times during pregnancy, we conducted intention-to-treat (ITT) and exposure-response (E-R) analyses to determine if the HAPIN intervention and corresponding HAP exposure was associated with the risk of fetal/neonatal outcomes. A total of 3200 women (mean age 25.4 ± 4.4 years, mean gestational age at randomization 15.4 ± 3.1 weeks) were included in this analysis. Relative risks for stillbirth, congenital anomaly and neonatal mortality were 0.99 (0.60, 1.66), 0.92 (95 % CI 0.52, 1.61), and 0.99 (0.54, 1.85), respectively, among women in the intervention arm compared to controls in an ITT analysis. Higher mean personal exposures to PM_2.5, CO and BC during pregnancy were associated with a higher, but statistically non-significant, incidence of adverse outcomes. The LPG stove and fuel intervention did not reduce the risk of these outcomes nor did we find evidence supporting an association between personal exposures to HAP and stillbirth, congenital anomalies and neonatal mortality.